PRESENTATION

1. REVIEW ARTICLES – AN OVER VIEW ENTEROCOCCAL RESISTANCE INDIAN JOURNAL MED ICROBIOLOGY 2005,VOL-23,PAGE214-219 (AVAILABLE FROM ON LINE) ABSTRACT: Nosocomial acquisition of microorganisms resistant to multiple antibiotics represents a threat to patient safety. Here we,

2. PRESENTATION ENTEROCOCCAL RESISTANCE- AN OVERVIEW

3. review the antimicrobial resistance in enterococcus, which makes it in important nosocomial pathogen. The emergence of enterococci with acquired resistance to vancomycin has been particularly problematic as it often occurs in enterococci that are also highly resistant to ampicillin and aminoglycoside thereby associated with devastating therapeutic

4. consequences. Multiple factors contribute to colonization and infectin with vancomycin resistant enterococci ultimately leading to environmental contamination and cross infection. Decreasing the prevalence of these resistant strains by multiple control efforts therefore, is of paramount importance.

5. KET WORD: Enterococci, antimicrobial resistance, therapeutic options, control efforts. INTRODUCTION: Enterococci, though commensals in adult faeces are important nosocomial pathogens. Their emergence in past two decades is in many respects attributable to their resistance to many commonly used antimicrobial agents

6. (aminoglycosides,cephalosporins, aztreonam, semisynthetic penicillin, trimethoprim-sulphamethoxazole) and ease with which they appear to attain and transfer resistant genes, thus giving rise to enterococci with high level aminoglycoside resistance(HLAR). ß-Lactamase production and glycopeptide resistance.

7. The most common nosocomial infections produced by these organisms are urinary tract infections (associated with instrumentation and antimicrobial administration), followed by intra-abdominal and pelvic infections. They also cause surgical wound infections, bacteraemia, endocarditis, neonatal sepsis and rarely meningitis.

8. E. Faecalis is the most common cause (80-90%) of infection followed by E. Faecium(10-15%). However erpergence of enterococci with multi drug resistance particularly to vancomycin is predominantly seen in E. faecium. Thus, this entity merits a complete description of antimicrobial resistance, current possibilities for treatment and variety of measures that may limit the proliferation of resistance within a health care environment.

9. ANTIMICROBIAL RESISTANCE Enterococci have a remarkable ability to survive in an environment of heavy antibioties. Indeed, it is the resistance of these organisms to multiple antimicrobial agents that makes them such feared opponents. Antimicrobial resistance in

10. enterococci is of two types: Inherent/ intrinsic resistance and acquired resistance. Intrinsic resistance is species characteristics and thus present in all members of species and is chromosomally mediated. On the other hand, acquired resistance results from either mutation in DNA or acquisition of new DNA.

11. RESISTANCE TO ß-LACTAMS INTRINSIC RESISTANCE: Enterococci begin with intrinsic resistance to most ß-lactum antibiotics because of low affinity penicillin binding proteins (PBPs), which enable them to synthesize cell wall components even in the presence of modest concentration of most ß-lactam antibiotics.

12. TOLERANCE In addition, enterococci are “ tolerant” to the activity of ß-Lactams, that is enterococci are inhibited but not killed by these agents. This property is an acquired characteristic.

13. ß-LACTAMASE ENZYME Enterococci, exclusively strains of E. faecalis, expressing ß-lactamase enzyme and having high level resistance to penicillin(HLPR) and it’s production is plasmid mediated. Isolates of E.faecium do not produce penicillinase yet confer high level resistance(HLR).

14. AMINOGLYCOSIDE RESISTANCE INTRINSIC RESISTANCE:Enterococci exhibit low level resistance to all aminoglycosides (MIC 8 to 256 mgm/ml) which appears to be due to low uptake of these agents. ACQUIRED RESISTANCE:Combination of penicillin plus streptomycin produced bactericidal killing of enterococci, until unfortunately, enterococci developed HLR to streptomycin.

15. HL.AR is being conducted by series of aminoglycoside modifying enzymes (AME) coded by plasmid and are transferable. GLYCOPEPTIDE RESISTANCE: Considerable consternation greeted the first report of appearance of VRE in 1980s, followed by its rapid spread.

16. COLONIZATION AND INFECTION Faecal carriage of VRE is recognized to be frequently associated with serious clinical infection and it is likely that colonization of gastrointestinal tract occurs as a prelude to clinical infection.

17. SCREENING METHODS FOR DETECTION OF VRE In the face of increasing rate of colonization with VRE and in the light of increasing concerns about the possible effect of this organism on patients with high risk of infections screening methods have been introduced for detection of VRE. The reliable and recommended agar screen method includes using brain heart infusion (BHI) agar with 6 mgm of vancomycin per ml. Growth indicates resistance and no growth indicates susceptibility.

18. THERAPEUTIC OPTIONS FOR MULTIPLY RESISTANT ENTEROCOCCI Enterococci have a vast potential for acquiring and disseminating resistant genes. As a result of this, they are currently causing significant therapeutic difficulties. Strains resistant to penicillin by ß-lactamase production respond to gentamicin plus ampicillin-sulbactam or ampicillin-clavulanate or vancomycin.

19. ß-lactam resistance without ß-lactamase production responds to vancomycin plus gentamicin. Management of clinical HLAR enterococcal infection is quite limited. Two newer agents with activity against VRE are quinopristin-dalfopristin and linezolid which are approved.

20. CONCLUSIONS During past two decades, enterococci resistant to multiple antimicrobial agents have been recognized, including strains resistant to vancomycin, ß-lactams and aminoglycosides, making it a formidable nosocomial pathogen. Thus is is crucial for laboratories to provide accurate antimicrobial resistance patterns for enterococci. THANK U TO ALL